HIV-1 RNA levels in blood samples taken at each visit were measured by the Abbott RealTime polymerase chain reaction (PCR) assay with a reliable lower limit of quantification of 40 copies/mL. The percentage of participants with HIV-1 RNA ≥50 copies/mL at Week 48 is presented using the FDA Snapshot missing data approach.

All randomized participants who received at least one dose of study intervention.

An AE was defined as any untoward medical occurrence in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. The percentage of participants who experienced at least one AE was reported.

All randomized participants who received at least one dose of study intervention.

An AE was defined as any untoward medical occurrence in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. The percentage of participants who discontinued study intervention due to an AE was reported.

All randomized participants who received at least one dose of study intervention.

HIV-1 RNA levels in blood samples taken at each visit were measured by the Abbott RealTime PCR assay with a reliable lower limit of quantification of 40 copies/mL. The percentage of participants with HIV-1 RNA <40 copies/mL or <50 copies/mL at Week 48 is presented using the FDA Snapshot missing data approach.

All randomized participants who received at least one dose of study intervention.

HIV-1 RNA levels in blood samples taken at each visit was measured by the Abbott RealTime PCR assay with a reliable lower limit of quantification of 40 copies/mL. The percentage of participants with HIV-1 RNA ≥50 copies/mL, <40 copies/mL, or <50 copies/mL at Week 96 is reported for Group 2 participants who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96. Per protocol, the percentage of participants with HIV-1 RNA ≥50 copies/mL, <40 copies/mL, or <50 copies/mL at Week 96 for Group 1 participants is a separate outcome measure and is presented later in the record.

The analysis population consisted of all randomized participants in Group 2 who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96 who received at least one dose of study intervention and had data available for this outcome measure. Per protocol, the percentage of participants with HIV-1 RNA ≥50 copies/mL, <40 copies/mL, or <50 copies/mL at Week 96 for Group 1 participants is a separate outcome measure and is presented later in the record.

HIV-1 RNA levels in blood samples taken at each visit was measured by the Abbott RealTime PCR assay with a reliable lower limit of quantification of 40 copies/mL. The percentage of participants with HIV-1 RNA ≥50 copies/mL, <40 copies/mL, or <50 copies/mL at Week 96 is reported for Group 1 participants. Per protocol, the percentage of participants with HIV-1 RNA ≥50 copies/mL, <40 copies/mL, or <50 copies/mL at Week 96 for Group 2 participants who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96 is a separate outcome measure and is presented earlier in the record.

The analysis population consisted of all randomized participants in Group 1 who received at least one dose of study intervention and had data available for this outcome measure. Per protocol, the percentage of participants with HIV-1 RNA ≥50 copies/mL, <40 copies/mL, or <50 copies/mL at Week 96 for Group 2 participants who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96 is a separate outcome measure and is presented earlier in the record.

Plasma CD4+ T-Cell Count was measured in cells/mm^3 for baseline and 48 weeks. Baseline measurements were defined as the Day 1 value of each participant. The percentage change from baseline to Week 48 is presented.

All randomized participants who received at least one dose of study intervention and who have baseline data.

Plasma CD4+ T-Cell Count was measured in cells/mm^3 for baseline and 96 weeks. Baseline measurements were defined as the Day 1 value of each participant. The mean percent change from baseline to Week 96 in CD4+ T-cell count is reported for Group 1 participants. Per protocol, the mean percentage change from baseline in CD4+ T-cell count at Week 96 for Group 2 participants was not planned or conducted.

The analysis population consisted of all randomized participants in Group 1 who received at least one dose of study intervention and had data, including baseline data, available for this outcome measure. Per protocol, the percentage change from baseline in CD4+ T-cell count at Week 96 for Group 2 participants was not planned or conducted.

Plasma CD4+ T-Cell Count was measured in cells/mm^3 for Week 48 and Week 96. The mean percent change from Week 48 to Week 96 is reported for Group 1 and Group 2 participants who delayed switch over from baseline ART to DOR/ISL Week 48 to Week 96.

The analysis population consisted of all randomized participants who received at least one dose of study intervention and had data available for this outcome measure for participants in Group 1 and participants in Group 2 who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96.

Viral drug resistance is defined as participants with confirmed HIV-1 RNA ≥400 copies/mL and/or genotypic or phenotypic analysis of data showing evidence of resistance to the study drug administered. The percentage of participants who demonstrated drug resistance at Week 48 is presented.

Participants who met the definition of confirmed virologic rebound (two consecutive [2 to 4 weeks apart] occurrences of HIV-1 RNA ≥200 copies/mL) at any time during the study or who discontinued study intervention for another reason and have HIV-1 RNA ≥200 copies/mL at the time of discontinuation. Participants for whom available genotypic or phenotypic data showed evidence of resistance, irrespective of viral load, were also included.

Viral drug resistance was defined as participants with confirmed HIV-1 RNA ≥400 copies/mL and/or genotypic or phenotypic analysis of data showing evidence of resistance to the study drug administered. The percentage of participants who demonstrate drug resistance at Week 96 is presented for Group 1 and Group 2 participants who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96. Per protocol, the percentage of participants with evidence of viral drug resistance-associated substitutions from week 0 to week 48 for Group 1 and Group 2 participants is a separate outcome measure and is presented earlier in the record.

Analysis population included participants with virologic rebound (2 repeated incidents of HIV-1 RNA ≥200 copies/mL, 2-4 weeks apart) or who discontinued study intervention with HIV-1 RNA ≥200 copies/mL. Participants with available data showing resistance, despite viral load, are included. Per protocol, percentage of participants with evidence of viral drug resistance associated substitutions from week 0 to week 48 for Groups 1 and 2 is a separate outcome measure reported earlier in the record.

Blood serum samples were taken at baseline and Week 24. Per protocol, this outcome analysis was conducted in participants on PI-containing regimens (including PI- and InSTI-containing regimens), excluding participants who took lipid-lowering therapy during the study. The fasting lipids consisted of fasting cholesterol, fasting high density lipoprotein (HDL) cholesterol, fasting low density lipoprotein (LDL) cholesterol, fasting non-HDL cholesterol, and fasting triglycerides. The mean change from baseline to Week 24 in fasting lipids is presented.

All randomized participants on PI-containing regimens (including PI- and InSTI-containing regimens) who received at least one dose of study intervention and had baseline and Week 24 data available for each lipid type, excluding participants who took lipid-lowering therapy during the study, per protocol.

Blood serum samples were taken at baseline and Week 24. Per protocol, this outcome analysis was conducted in participants on InSTI-based regimens (non-PI containing regimens), excluding participants who took lipid-lowering therapy during the study. The fasting lipids consisted of fasting cholesterol, fasting HDL cholesterol, fasting LDL cholesterol, fasting non-HDL cholesterol, and fasting triglycerides. The mean change from baseline to Week 24 in fasting lipids is presented.

All randomized participants on InSTI-based regimens (non-PI containing regimens) who received at least one dose of study intervention and had baseline and Week 24 data available for each lipid type, excluding participants who took lipid-lowering therapy during the study, per protocol.

Blood serum samples were taken at baseline and Week 24. Per protocol, this outcome analysis was conducted in participants on all other non-PI- and non-InSTI containing regimens, excluding participants who took lipid-lowering therapy during the study. The fasting lipids consisted of fasting cholesterol, fasting HDL cholesterol, fasting LDL cholesterol, fasting non-HDL cholesterol, and fasting triglycerides. The mean change from baseline to Week 24 in fasting lipids is presented.

All randomized participants on all other non-PI- and non-InSTI containing regimens, who received at least one dose of study intervention and had baseline and Week 24 data available for each lipid type, excluding participants who took lipid-lowering therapy during the study, per protocol.

Blood serum samples were taken at baseline and Week 48. Per protocol, this outcome analysis was conducted in participants on PI-containing regimens (including PI- and InSTI-containing regimens), excluding participants who took lipid-lowering therapy during the study. The fasting lipids consisted of fasting cholesterol, fasting high density lipoprotein (HDL) cholesterol, fasting low density lipoprotein (LDL) cholesterol, fasting non-HDL cholesterol, and fasting triglycerides. The mean change from baseline to Week 48 in fasting lipids is presented.

All randomized participants on PI-containing regimens (including PI- and InSTI-containing regimens) who received at least one dose of study intervention and had baseline and Week 48 data available for each lipid type, excluding participants who took lipid-lowering therapy during the study, per protocol.

Blood serum samples were taken at baseline and Week 48. Per protocol, this outcome analysis was conducted in participants on InSTI-based regimens (non-PI containing regimens), excluding participants who took lipid-lowering therapy during the study. The fasting lipids consisted of fasting cholesterol, fasting HDL cholesterol, fasting LDL cholesterol, fasting non-HDL cholesterol, and fasting triglycerides. The mean change from baseline to Week 48 in fasting lipids is presented.

All randomized participants on InSTI-based regimens (non-PI containing regimens) who received at least one dose of study intervention and had baseline and Week 48 data available for each lipid type, excluding participants who took lipid-lowering therapy during the study, per protocol.

Blood serum samples were taken at baseline and Week 48. Per protocol, this outcome analysis was conducted in participants on all other non-PI- and non-InSTI containing regimens, excluding participants who took lipid-lowering therapy during the study. The fasting lipids consisted of fasting cholesterol, fasting HDL cholesterol, fasting LDL cholesterol, fasting non-HDL cholesterol, and fasting triglycerides. The mean change from baseline to Week 48 in fasting lipids is presented.

All randomized participants on all other non-PI- and non-InSTI containing regimens, who received at least one dose of study intervention and had baseline and Week 48 data available for each lipid type, excluding participants who took lipid-lowering therapy during the study, per protocol.

Baseline measurements were defined as the Day 1 value of each participant. The change from baseline in body weight to Week 48 is presented for participants who received InSTI- based regimens.

All randomized participants who received at least one dose of study intervention, had baseline and Week 48 data available for body weight, and received InSTI-based regimens.

An AE was defined as any untoward medical occurrence in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. The percentage of participants who experienced at least one AE up to Week 96 is reported for Group 1 participants. Per protocol, the percentage of participants with one or more AEs for Group 2 participants is a separate outcome measure and is presented later in the record.

The analysis population consisted of all randomized participants in Group 1 who received at least one dose of study intervention. Per protocol, the percentage of participants with one or more AEs for Group 2 participants is a separate outcome measure and is presented later in the record.

An AE was defined as any untoward medical occurrence in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. The percentage of participants who discontinued study intervention due to an AE up to Week 96 is reported for Group 1 participants. Per protocol, the percentage of participants who discontinued study intervention for Group 2 participants is a separate outcome measure and is presented later in the record.

The analysis population consisted of all randomized participants in Group 1 who received at least one dose of study intervention. Per protocol, the percentage of participants who discontinued study intervention for Group 2 participants is a separate outcome measure and is presented later in the record.

An AE was defined as any untoward medical occurrence in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. The percentage of participants who experienced at least one AE from Week 48 up to Week 96 is reported for Group 1 participants and Group 2 participants who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96.

The analysis population consisted of all randomized participants who received at least one dose of study intervention for participants in Group 1 and participants in Group 2 who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96.

An AE was defined as any untoward medical occurrence in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. The percentage of participants who discontinued study intervention due to an AE from Week 48 up to Week 96 is reported for Group 1 participants and Group 2 participants who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96.

The analysis population consisted of all randomized participants who received at least one dose of study intervention for participants in Group 1 and participants in Group 2 who delayed switch over from baseline ART to DOR/ISL from Week 48 to Week 96.